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Autoimmune Hemolytic Anemia

Hemolytic anemia is characterized by intravascular and extravascular destruction of erythrocytes. It manifests if the production of the erythrocytes in the bone marrow is slower than their degradation. A first good differentiation of the several forms of hemolytic anemia can be made between ‘hereditary’ and ‘acquired’. In this article, the most important forms of hereditary and acquired hemolytic anemia are presented, emphazising on their etiology, clinic and therapy.

Hemolytic anemia is characterized by intravascular and extravascular destruction of erythrocytes. It manifests if the production of the erythrocytes in the bone marrow is slower than their degradation. A first good differentiation of the several forms of hemolytic anemia can be made between ‘hereditary’ and ‘acquired’. In this article, the most important forms of acquired hemolytic anemia are presented, emphasizing on their etiology, clinic and therapy.

00:01
Looking at autoimmune hemolytic anemia, one
can identify two types of autoantibody.
00:10
The cold antibodies are anti red blood cell autoantibodiesthat only bind at significantly below normal body temperature.
00:20
And therefore the extremities
are particularly affected.
00:24
These antibodies are
usually of the IgM class.
00:28
In contrast, the warm type antibodies
found in autoimmune hemolytic anemia areanti red blood cell autoantibodies
that bind at normal body temperatures.
00:39
And these are usually
of the IgG class.
00:44
Following binding of IgM or IgG autoantibodies to
the surface of the red blood cells, the classicalpathway of complement can become activated leading
to the generation of the membrane attack complex.
01:01
This will cause lysis
of the red blood cells.
01:07
In addition, phagocytic cells with Fc receptors on
their cell surface can take up erythrocytes thathave been coated with antibody, and this again will
lead to the destruction of those red blood cells.
01:26
One can test for the presence of these
autoantibodies using a test called the Coombs test.
01:32
And there are two different
versions of this test.
01:36
In the direct test, one takes a blood
sample from the patient and looks forthe presence of autoantibodies that are
already coating the red blood cells.
01:50
And one detects the presence of these
autoantibodies that have already coatedthe red blood cells, using a second
antibody - an anti-human immunoglobulin.
02:02
This will cross link together the
antibodies on the surface of the redblood cells causing agglutination
which can be visualized by the eye.
02:15
In the indirect test, one looks for
the presence of the autoantibodyitself, free autoantibody that
is not bound to the erythrocytes.
02:27
One can take this antibody from the serum
of patients, mix it with red blood cells.
02:34
And if the autoantibody has
specificity for red blood cells, thisanti red blood cell autoantibody
will bind to the red blood cells.
02:43
And this autoantibody can then again be detected by
using a second antibody, an anti-human immunoglobulin.
02:51
So this is the indirect Coombs test.
02:54
And again, upon adding the anti-human
immunoglobulin, there will be agglutination whichcan be visualized by simply looking at the
slide on which this test is being carried out.
03:05
In pernicious anemia, there is a autoimmune attack that
prevents the absorption of vitamin B12 from the gut.
03:17
So in the normal individual, ingested vitamin B12
is picked up by intrinsic factor in the stomach.
03:26
And this complex of vitamin B12 bound
to intrinsic factor is then absorbedfrom the gut and can be used in the
development of red blood cells.
03:39
However in pernicious anemia, there
are autoantibodies being produced.
03:45
One of those autoantibodies is against
the parietal cell H+ K+ ATPase.
03:53
This leads to a reduced
production of intrinsic factor.
03:58
And there are also autoantibodies
against intrinsic factor itself.
04:03
This means that vitamin B12 is not
absorbed from the gut resulting in anemia.
04:10
In autoimmune thrombocytopenic
purpura, platelets are affected.
04:17
There are autoantibodies to the platelet
glycoproteins GPIIb-IIIa and GPIb-IX.
04:28
These are removed and destroyed by splenic
macrophages and liver Kupffer cells.
04:35
So following binding of these
autoantibodies to the platelets, the complexof the autoantibody together with
the platelet is recognized by Fcgamma receptors on the surface of these
phagocytic cells and the plateletsare destroyed, resulting in autoimmune thrombocytopenic purpura.

About the Lecture

The lecture Autoimmune Hemolytic Anemia by Peter Delves, PhD is from the course Hypersensitivity and Autoimmune Disease. It contains the following chapters:

Autoimmune Hemolytic Anemia

Pernicious Anemia

Autoimmune Thrombocytopenic Purpura

Included Quiz Questions

The ‘cold’ antibodies which cause autoimmune hemolytic anemia are of which antibody class?

IgM

IgG

IgA

IgD

IgE

A Direct Coombs test detects...?

Anti-RBC autoantibody that is already bound to RBCs using an anti-Human Ig

Destroyed or damaged RBCs

Free anti-RBC autoantibody in serum that is mixed with RBCs

An exaggerated antibody response to anti-Human Ig

Anti-RBC autoantibody by injecting patient with anti-human Ig

Which of the following auto-antibodies would be present in someone suffering from Pernicious anemia?

Anti-Intrinsic factor and Anti-parietal cell H+K+ ATPase.

Anti-B12 and Anti-Intrinsic factor.

Anti-B12 and Anti-parietal cell H+K+ ATPase.

Anti-Human Ig and Anti-Intrinsic factor.

Anti-parietal cell and Anti-Human Ig.

Which of the following platelet glycoproteins is effected in autoimmune thrombocytopenic purpura?

GPIIb-IIIa

Fcγ

Intrinsic factor

GPx-IIb

IgM

Author of lecture Autoimmune Hemolytic Anemia

Peter Delves, PhD

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